Circulatory shock remains a leading cause of death in both military and civilian trauma. Early, accurate and reliable prediction of decompensation is necessary for the most efficient interventions and clinical outcomes. Individual tolerance to reduced central blood volume can serve as a model to assess the sensitivity and specificity of vital sign measurements. The compensatory reserve (CRM) is the measurement of this capacity. Measurements of muscle oxygen saturation (SmO2), blood lactate, and end tidal CO2 (EtCO2) have recently gained attention as prognostic tools for early assessment of the status of patients with progressive hemorrhage, but lack the ability to adequately differentiate individual tolerance to hypovolemia. We hypothesized that the CRM would better predict hemodynamic decompensation and provide greater specificity and sensitivity than metabolic measures. To test this hypothesis, we employed lower body negative pressure on healthy human subjects until symptoms of presyncope were evident. Receiver operating characteristic area under the curve (ROC AUC), sensitivity, and specificity were used to evaluate the ability of CRM, partial pressure of oxygen (pO2), partial pressure of carbon dioxide (pCO2), SmO2, lactate, EtCO2, potential of hydrogen (pH), base excess and hematocrit (Hct) to predict hemodynamic decompensation. The ROC AUC for CRM (0.94) had a superior ability to predict decompensation compared with pO2 (0.85), pCO2 (0.62), SmO2 (0.72), lactate (0.57), EtCO2 (0.74), pH (0.55), base excess (0.59), and Hct (0.67). Similarly, CRM also exhibited the greatest sensitivity and specificity. These findings support the notion that CRM provides superior detection of hemodynamic compensation compared with commonly used clinical metabolic measures.

Based on evidence extracted from a cross-sectional review of the literature, we sought to advance a novel conceptual framework that the physiology of hemorrhagic shock from exsanguination and maximal oxygen uptake ([Formula: see text]O2max), induced by physical exercise, shares key common features. As such, this review focuses on the notion that intolerance to inadequate oxygen delivery (DO2) resulting from associated states of hypovolemia appears to be a common physiological link that “connects” hemorrhagic shock to the physiology that limits maximal aerobic capacity. Our approach focuses on the similarities in a complex cascade of cardiopulmonary, metabolic and autonomic compensatory responses during hemorrhage and maximal physical exertion that ultimately function to avoid critical levels of DO2 (DO2crit) and are manifested by elevation in blood lactate levels. We introduce a paradigm of absolute (i.e. hemorrhage) versus relative (i.e. exercise) hypovolemia as a primary physiological factor that contributes to reaching DO2crit, and define the concept of “O2 deficit” to replace the clinical concept of O2 debt. Using the peer-reviewed literature, we provide human data obtained from patients who suffered hemorrhagic shock from severe blood loss and compare it to healthy subjects who performed maximal exercise. We include a novel conceptual framework of the continuum of metabolic relationship between DO2 and [Formula: see text]O2 that is manifested as the final step during both progressive blood loss leading to hemorrhagic shock and at [Formula: see text]O2max. We present evidence to support the contribution of utilizing “O2 extraction reserve” as the initial mechanism for developing an O2 deficit, and the notion of individual variability in compensatory responses. In the absence of reversing inadequate DO2, an increased reliance on O2 extraction reserve, cellular anaerobic glycolysis, and phosphocreatine stores to supplement the energy required by the tissues for normal function will deplete a finite capacity for compensation. In the end, acidity reflected by a blood pH ≤ ∼7.0 leads to disturbance of normal cell functioning of metabolic machinery manifested by irreversible shock in the case of hemorrhage or physical exhaustion when [Formula: see text]O2max is reached. Impact statement Disturbance of normal homeostasis occurs when oxygen delivery and energy stores to the body’s tissues fail to meet the energy requirement of cells. The work submitted in this review is important because it advances the understanding of inadequate oxygen delivery as it relates to early diagnosis and treatment of circulatory shock and its relationship to disturbance of normal functioning of cellular metabolism in life-threatening conditions of hemorrhage. We explored data from the clinical and exercise literature to construct for the first time a conceptual framework for defining the limitation of inadequate delivery of oxygen by comparing the physiology of hemorrhagic shock caused by severe blood loss to maximal oxygen uptake induced by intense physical exercise. We also provide a translational framework in which understanding the fundamental relationship between the body’s reserve to compensate for conditions of inadequate oxygen delivery as a limiting factor to [Formula: see text]O2max helps to re-evaluate paradigms of triage for improved monitoring of accurate resuscitation in patients suffering from hemorrhagic shock.

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